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1 (such as PI3K) leading to the inhibition of histone deacetylase 2.
2 rescued by the simultaneous decrease of the Histone Deacetylase 2.
3 se in levels of the memory repressor protein histone deacetylase 2.
4 uding BRG1, BRM, hSNF2H, BAF155, mSin3a, and histone deacetylase 2.
5 dent repression domain, which interacts with histone deacetylase 2.
6 icosteroid resistance though inactivation of histone deacetylase 2.
7 of brain sections showed that TopIIbeta and histone deacetylase 2, a known TopIIbeta-interacting pro
8 ed inflammatory genes through recruitment of histone deacetylase-2, activating anti-inflammatory gene
9 effect may be due to inhibition of PDE4 and histone deacetylase-2 activation, resulting in switching
10 of 1) chromatin perturbation by mutation of histone deacetylases, 2) activation of Snf1, and 3) the
12 ardiac function via p27/casein kinase-2alpha/histone deacetylase 2 and indicate that mutations within
13 e demonstrate that Hu proteins interact with histone deacetylase 2 and inhibit its deacetylation acti
14 nflammation enhanced the interaction between histone deacetylase 2 and methyl-CpG-binding protein 2,
15 1 and methylated CpG binding protein 2 with histone deacetylase 2 and of REST with histone deacetyla
16 r the development of selective inhibitors of histone deacetylase 2 and suggest that cognitive capacit
17 progression, where it interacts with class I histone deacetylases 2 and 3 (HDAC2 and HDAC3) to regula
18 eacetylase 1 but had no effect on binding to histone deacetylases 2 and 3, the coactivator p300, or e
19 stem, we design cyclic peptides that inhibit histone deacetylases 2 and 6 (HDAC2 and HDAC6) with enha
20 select chromatin regulators (e.g., ARID1A/B, histone deacetylase 2, and HCF1), mutations of which und
21 and increased methyl-CpG binding protein-2, histone-deacetylase-2, and switch-independent-3a binding
23 rodegeneration, and a human homolog of RPD3, histone deacetylase 2, bound ATM and abrogated ATM activ
25 anscription, and FosB in turn, utilizes FosB/histone deacetylase 2 complex to repress E-cadherin expr
26 de novo methylation of the promoter, whereas histone deacetylase 2 cooperates with DNMT1 to inhibit t
27 sor 1, methylated CpG binding protein 2, and histone deacetylase 2 enrichment, but not of sirtuin 1 o
31 NF-kappaB) pathway, as an LRA and identified histone deacetylase 2 (HDAC2) and bromodomain-containing
32 ubiquitin ligase activity, by recruiting the histone deacetylase 2 (HDAC2) and CCAAT/enhancer-binding
33 , and mice suggested that cross-talk between histone deacetylase 2 (HDAC2) and DNA methyltransferase
34 ng molecule that mediates S-nitrosylation of histone deacetylase 2 (HDAC2) and epigenetic changes in
37 , we demonstrate that epigenetic regulator's histone deacetylase 2 (HDAC2) and polycomb repressive co
38 e nucleus, accompanied by S-nitrosylation of histone deacetylase 2 (HDAC2) and Sirtuin 1 (SIRT1), dea
40 expression by recruiting chromatin modifier histone deacetylase 2 (HDAC2) as revealed by chromatin i
41 lying mechanism involves recruitment of MTA1-histone deacetylase 2 (HDAC2) complexes onto two selecti
42 previously shown that subunits of the mSin3A/histone deacetylase 2 (HDAC2) corepressor complex copuri
43 onstrate that the chromatin-modifying enzyme histone deacetylase 2 (Hdac2) functions with a small hom
45 triggers NO synthesis and S-nitrosylation of histone deacetylase 2 (HDAC2) in neurons, resulting in c
46 ilencing of histone deacetylase 1 (Hdac1) or histone deacetylase 2 (Hdac2) in OPCs did not affect BMP
47 ation is associated with decreased levels of histone deacetylase 2 (HDAC2) in the nucleus accumbens.
51 ressor complexes containing PRMT5 and either histone deacetylase 2 (HDAC2) or HDAC3, enhanced binding
52 estingly, we found that limiting endothelial histone deacetylase 2 (HDAC2) prevented cerebral ECs fro
53 ng to the glucocorticoid response element of histone deacetylase 2 (HDAC2) promoter, resulting in the
54 ted by acetylation of core histones, whereas histone deacetylase 2 (HDAC2) suppresses inflammatory ge
56 es FOXM1 bound to the FHRE before recruiting histone deacetylase 2 (HDAC2) to the promoter, leading t
58 d the glucocorticoid receptor (GR-alpha) and histone deacetylase 2 (HDAC2), a corepressor important f
59 s of inhibitor kappaB-alpha (IkappaB-alpha), histone deacetylase 2 (HDAC2), acetylated (ac-) histone
60 bromodomain-containing protein 4 (BRD4) and histone deacetylase 2 (HDAC2), along with ubiquitin-spec
61 luding methyl-CpG binding protein 2 (MeCP2), histone deacetylase 2 (HDAC2), and SIN3 transcription re
62 ted to its N-terminal domain, which recruits histone deacetylase 2 (Hdac2), as demonstrated by (i) im
63 l splicing variant in the mouse kidney) with histone deacetylase 2 (HDAC2), as well as the function o
64 ition controlled by the epigenetic regulator histone deacetylase 2 (HDAC2), which controls endothelia
65 istance is largely caused by inactivation of histone deacetylase 2 (HDAC2), which is critical for the
66 munoprecipitation assay experiments revealed histone deacetylase 2 (HDAC2)-MTA1 protein-protein inter
70 cription factor activator protein 1, reduced histone deacetylase-2 (HDAC2) expression, raised macroph
71 ve inflammation via reduced transcription of histone deacetylase-2 (HDAC2) in lung epithelial and mac
74 oter by binding to nearby DNA and recruiting histone deacetylase-2 (HDAC2) to reduce histone acetylat
76 yperacetylation and diminished enrichment of histone deacetylase-2 (HDAC2), but not HDAC3, at the Cac
77 4 (also called Mi-2beta) is a component of a histone-deacetylase-2 (HDAC2)-containing complex, the nu
78 (CoREST), histone deacetylase 1 (HDAC1), and histone deacetylase 2 in erythroleukemia and T cell leuk
79 e repressor CoREST (also known as RCOR1) and histone deacetylase 2 in these early dividing cells; and
80 at the essential nuclear gene, P. falciparum histone deacetylase 2 (PfHda2), is a global silencer of
81 AR formed a repressive complex by recruiting histone deacetylase 2 to the SIRT3 promoter, and depleti
82 ownstream molecules casein kinase-2alpha and histone deacetylase 2 were significantly elevated in Eya